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Definition of Terms v Cardiac output – Quantity of blood pumped by the LV into the aorta each minute (NV = 5L/min) v Cardiac index – CO/m2 (NV = 3.4L/min/m2; range of 2.8-4.2) v Stroke volume – End diastolic volume – End systolic volume v Ejection fraction – (SV/EDV) * 100 (NV = 60-75%) Regulatory factors of myocardial contraction v Preload Load before ventricular contraction Physiologically, the venous returne The LVEDP Wall stress at the end of diastole v Afterload The force resisting shortening of the myofibrils v Contractility Inotropic state Accounts for alteration of performance induced by hormonal and biochemical change Increased when there is enhanced interaction between calcium and contractile protein Mechanisms of cardiac reserve v Increased heart rate Trained athletes = 200-230/minute Normal young individuals = 170=180/min Old, untrained, with heart disease = 120-140/min v Increased stroke volume EF = 60-75% Normal < 55% Systolic dysfunction < 40% Depressed < 20% Severely depressed v Increased oxygen extraction v Redistribution of blood flow Local autoregulation Integrated response of the CNS v Anaerobic metabolism – 5-30% of energy requirement v Cardiac dilation v Cardiac hypertrophy
Heart Failure Definition v It is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood v Heart failure is preferred over CHF because not all patients are volume overload at the time of initial evaluation v Clinical syndrome of HF may result from disorder of the pericardium, myocardium or endocardium, or great vessels but majority of patients have symptoms due to impairment of LV function v Cannot be assessed with precision – accurate estimates of prevalence, incidence, and prognosis are lacking v Incidence – average annual incidence per 1000
Age 45-54 55-64 65-74 75-84 85-94 Men 2 4 9 18 39 Women 1 2 6 12 31
NYHA Functional Classification Asymptomatic during daily usual No limitation I activity Symptoms during ordinary daily II Slight limitation activity Symptoms noted during minimal III Moderate activity limitation IV Severe limitation Symptoms persist even at rest Cardiovascular Diagnosis v Etiologic v Anatomic v Physiologic v Functional Capacity (I-IV) v Objective Assessment No objective evidence of CVD Objective evidence of minimal CVD Objective evidence of moderately severe CVD Objective evidence of severe CVD Stages
Stage A Stage B Stage C Stage D High risk for developing HF but has no structural disorder of the heart Structural disorder of the heart but who has never developed symptoms of HF Past or current symptoms of HF associated with underlying structural heart disease (symptomatic) End-stage disease who requires specialized treatment strategies (recurrent HF)
Mechanisms of Cardiac Reserve v 24% - Splanchnic v 19% - Renal v 21% - Skeletal v 9% - Skin v 10% - Other v 13% - Cerebral, Coronary Laplace’s Law v Wall stress = Pressure x Radius 2 x wall thickness v As the pressure increases (ie. Due to aortic stenosis), thickness of the LV increases in order to offset the pressure overload; and wall stress remains normal)
Examples v Stage A Systemic HPN CAD DM Cardiotoxic drug therapy or alcohol abuse Personal history of rheumatic fever Family history of cardiomyopathy v Stage B LVH or fibrosis LV dilatation or hypocontractility Asymptomatic valvular heart disease Previous myocardial infarction v Stage C Dyspnea or fatigue due to LV systolic dysfunction Asymptomatic patients who are undergoing treatment for prior symptoms of HF v Stage D End stage disease who requires specialized treatment strategies such as mechanical circulatory support, continuous inotropic infusions, cardiac transplantation, or hospice care
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occasionally by months or even years Continues after the appearance of symptoms May contribute importantly to worsening of symptoms despite treatment v Factors that contribute to LV remodeling Neurohormones and cytokines Increased LV volume and pressure Myocardial cell elongation Replacement and reactive collaged deposition (ie. and cool extremities v Chronic HF – punctuated by exacerbations v Right HF – syndromes presenting predominantly with congestion of the systemic circulation v Left HF – syndromes presenting predominantly with congestion of the pulmonary circulation v Principal hallmark of HF Systolic dysfunction: depressed LV EF (<40%) Diastolic dysfunction: normal EF with impairment of one ore more indices of ventricular filling v Etiologies Ischemic Nonischemic Ø Unspecified Ø Specified ♥ Idiopathic ♥ Valvular ♥ Hypertensive ♥ Ethanol ♥ Vital ♥ Postpartum ♥ Amyloidosis ♥ Others Ischemic cascade v Coronary artery occlusion v Diastolic abnormalities v Systolic abnormalities v Perfusion defects v Hemodynamic abnormalities v ECG changes v Angina HF as a progressive disorder v LV dysfunction begins with some injury to the myocardium and is usually a progressive process. which ultimately results in a change in the geometry of the LV such that the chamber dilates. the activation of the rennin-angiotensin and sympathetic nervous systems. hypertrophies. and becomes more spherical v Cardiac remodeling Generally precedes the development of symptoms. oliguria. Increased collagen turnover) Myocyte slippage secondary to dissolution of collagen struts Apoptosis Necrosis Myocardial infarct expansion Dilation and reshaping of the LV 2 Lala 3C-Med-09 . and eventually sodium and water retention Frank-Starling’s Law v Intrinsic ability of the heart to adapt itself to changing loads of inflowing blood v Within physiologic limits. edema Low cardiac output Diastolic dysfunction Increasing symptoms Heart failure v Acute heart failure – acute dyspnea with signs of pulmonary congestion including pulmonary edema v Cardiogenic shock – low arterial pressure. the heart pumps all the blood that comes to it without allowing excessive damming of blood in the veins v Heterometric autoregulation Cardiovascular continuum Index Event Acute MI Gene mutation Acute inflammation Onset of HPN Valvular Heart Disease Others Structural remodeling and progression of disease Myocyte hypertrophy Fibrosis. which occurs in association with homeostatic attempts to decrease wall stress through increases in wall thickness. chamber dilatation Collagen shunt dissolution Cell drop out (apoptosis) Cell necrosis Neuroendocrine activation Cytokine release Increased wall stretching Chamber dysfunction Clinical syndrome of HF Salt and water retention Congestion. This leads to fall in tissue perfusion. Examples are patients Ø Frequently hospitalized for HF or cannot be safely discharged from the hospital Ø In the hospital awaiting heart transplantation Ø At home receiving continuous intravenous support for symptom relief or being supported with a mechanical circulatory assist device Ø In a hospice setting for management of HF Acute MI v 20-25% LV mass infarcted = LV dysfunction v >40% LV mass infracted = cardiogenic shock Systolic HF v Impaired contractility leads to reduction in cardiac output. even in the absence of a new identifiable insult to the myocardium v The principal manifestation of such progression is a process known as remodeling.
Vascular Pathophysiology of HF Consequences of neurohormonal stimulation in HF Consequence of Neurohormonal Stimulation Pathophysiology Terminal events in HF v Systemic organ failure v Pulmonary/ cerebral embolus v Lethal arrhythmias Neuroendocrine factors known to be increased in HF Endothelin Norepinephrine Beta-endorphins Epinephrine Calcitonin gene-related peptide Renin activity Growth hormone Angiotensin II Cortisol Aldosterone TNF – alpha Arginine vasopressin Neurokinin A Neuropeptide Y Substance P VIP Adrenomedullin Prostaglandins Brain natriuretic peptide Atrial natriuretic factor Assessment of patients with HF v History and PE v Diagnostic Studies Laboratory tests Electrocardiography CXR Exercise testing ECG Radionucleotide imaging Cardiac catheterization Endomyocardial biopsy 3 Lala 3C-Med-09 .
sweating. rising movement v Sustained AB LV outflow obstruction Systemic HPN Depressed systolic function v Hepatojugular/ abdominojugular refex Firm. sustained upper abdominal pressure Patient breathing quietly Normal transient 1cm JVP increase HF: sustained elevation of JVP v Cardiovascular edema History of HPN/ heart disease Primarily complaining of SOB Peripheral Chest X-ray v Cardiomegaly v Hilar vascular congestion v Bronchial cuffing v Cephalization of vessels v Kinsley lines Echocardiography v Advantages Permits concomitant assessment of valvular disease. wheezing. loss of appetite) PE findings in HF v Elevated JVP or positive abdominal jugular reflex v A third heart sound v The third heart sound v Murmurs Displaced AB v Rales that do not disappear with cough v Peripheral edema v Narrow pulse pressure Right Heart Failure Cyanosis Increased JVP Hepatomegaly Ascites Dependent edema CXR: marked RV dilatation Left Heart Failure Dyspnea Orthopnea CXR: Pulmonary congestion Dependent edema Facial edema Ascites Hypoalbuminemia Proteinuria Cardiac Severe Absent Absent/ mild Absent Absent/ trace Hepatic Moderate Absent Severe Moderate/ Mild Absent/ trace Renal Mild Severe/ moderate Absent/ mild Severe Severe CHF Diagnostic Criteria (Framingham) Requires 1 Major and 2 Minor Criteria Major PND Neck vein distention Rales Cardiomegaly Acute pulmonary edema S3 gallop Venous pressure >16cm H20 (+) Hepatojugular reflux Minor Extremity edema Night cough Dyspnea on exertion Hepatomegaly Pleural effusion Reduced vital capacity Tachycardia (>120/min) Weight loss >4. tapping Sustained: plateau. with thyroid disease or age > 65) Electrocardiogram Abnormal T4 or TSH Acute ST-T wave changes Atrial fibrillation. other tachyarrhythmia Bradyarrhythmia Previous MI (eg. loss of capability for effective redistribution of systemic blood flow v Weakness v PND Onset is 2-5 hours after sleeping Relief 15-30 minutes after sitting/standing Accompanied by cough. and LA size Less expensive than radionucleotide ventriculography in most areas Able to detect pericardial effusion and ventricular thrombus More generally available 4 Lala 3C-Med-09 .5 kg over 5 days treatment Laboratory Tests Test recommendation CBC Finding Anemia Suspected HF due to or aggravated by decreased O2carrying capacity Nephritic syndrome Glomerulonephritis Volume overload due to renal dysfunction Increased extravascular volume due to hypoalbuminemia HF due to or aggravated by hypo/ hyperthyroidism Myocardial ischemia Thyroid disease or HF due to rapid ventricular rate HF due to low heart rate HF due to reduced contractile tissue Pericardial effusion Diastolic dysfunction Urinalysis Serum creatinine Serum albumin Proteinuria RBCs or cellular casts Elevated failure Decreased T4and TSH (only if atrial fibrillation. abdominal pain. anxiety v Orthopnea Dyspnea on recumbent position. bloating. altered mental status or fatigue in an elderly patient v Abdominal symptoms (eg. LVH. relieved by sitting or standing v Dyspnea on exertion v Decreased exercise tolerance Mechanisms responsible for exercise intolerance in patients with chronic HF have not been clearly defined Ø Very low EF – may be asymptomatic Ø Preserved EF – may have severe disability The cause of this discordance is not well understood v Unexplained confusion. Nausea. diuretics and digitalis May be accompanied by wheezing v Fatigue Deconditioning – inactivity or prolonged bed rest.Cardinal Manifestations/ Symptoms of HF v Dyspnea Any abnormally uncomfortable awareness of breathing Usually exertional May develop at rest Relieved by rest. Q wave) left ventricular performance Low voltage LVH PE findings v CAP assessment Normal: brisk. dome-shaped.
8 mEq/L) in patients with mild to moderate HF The ACC/AHA guidelines recommended the use of low doses of spirinolactone (25-50 mEq/day) in patients with recent or current NYHA Class IV HF.v Disadvantages Difficult to perform in patients with lung disease Usually only semiquantitative estimate of ejection fraction provided Technically inadequate in up to 18% of patients under optimal circumstances Radionucleotide ventriculogram v Advantages More precise and reliable measurement of EF Better assessment of right ventricular function v Disadvantages Requires venipuncture and radiation exposure Limited assessment of valvular heart disease and LVH Vascular Pathophysiology v Vasoconstricting systems Atrial Natriuretic Peptide (ANP) Ø Released from the atria (sometimes the ventricle) in response to volume expansion (stretch) Ø ANP ANP receptor guanylate cyclase cGMP ♥ Inhibit RAS and inhibit sympathetic activity vasodilator ♥ Promotes sodium excretion natriuresis and diuresis Brain Natriuretic Peptide (BNP) Ø Released from the brain (and ventricle) in response to volume expansion (stretch) Ø Diagnosis of HF Ø Screening for diastolic HF Ø Predictor of HF Ø Prognosis of HF Ø Guide to therapy of HF Ø Prognosis in ACS Ø BNP > 100pg/mL = HF ♥ Sensitivity – 90% ♥ Specificity . Start with low dose Digoxin – to those who continue to have symptoms despite above regimen. hyperuricemia. Spirinolactone. hyponatremia Ø Dehydration and postural hypotension Ø Hypocalcemia (in contrast to thiazides) Ø Hypersensitivity Ø Ototoxicity (if given by rapid IV bolus) v Deleterious effects of aldosterone Vascular inflammation and injury Potassium and magnesium loss Central hypertensive effects Endothelial dysfunction Ventricular arrhythmias Sodium retention Catecholamine potentiation Myocardial fibrosis Prothrombotic effects Specialized therapy for refractory HF v Systemic Factors causing HF Inappropriate medications Superimposed infection Anemia Uncontrolled diabetes Thyroid function Electrolyte disorders Pregnancy Stop smoking Limit alcohol intake Decrease salt intake : 2 to 3g sodium/day Restrict water intake Daily weight monitoring Cardiac rehab. eplerenone Compete with aldosterone for the mineralocorticoid receptor Prolong survival in selected patients Eplerenone more specific for mineralocorticoid receptor than spirinolactone. ARB.specific 5 v Potassium sparing diuretics Eg. a serum creatinine concentration < 2. Sodium nitroprusside v ACE Inhibitor All patients with asymptomatic or symptomatic LV dysfunction should be started on an ACEI Lala 3C-Med-09 . revascularization Valvular heart disease – surgery Cardiomyopathy . and for rate control of AF with RVR ARB – added to above regimen for Class II and III. hyperglycemia.5 mg/dL and a serum potassium < 5 mEq/L v Vasodilators – ACEI. program for stable patients v Lifestyle modification v Treatment of the cause HPN Coronary heart disease – medications. hypercholesteronemia.76% Ø Predictive accuracy of 83% General Principles of Treatment v General Principles of Treatment Correction of systemic factors Lifestyle modification Review drugs that my contribute to HF Treatment of the cause of HF Pharmacologic therapy Ø Relief of symptoms Ø Slow progression Ø Improve survival v Pharmacologic Therapy Improvement of symptoms Ø Ø Ø Ø Ø Ø Ø Ø Ø Digoxin Diuretics Beta blockers ACEI ARB ACEI ARB Beta blockers Spirinolactone/ eplerenone Prolongation of patient survival Diuretics – mainly to relieve symptoms ACEI – given with or after optimization of diuretic therapy Beta-blockers initiated after stabilization with ACEI. spirinolactone and eplerenone for Class IV patients Hydralazine and nitrates may be an alternative to ARB in black patients Pharmacologic therapy v Diuretics Helps reduce the amount of water in the body Adverse effects of loop diuretics (similar to thiazides in may respects) Ø Hypokalemia. less side effects Mild diuretics To improve survival in patients with recent or current NYHA class IV symptoms (RALES trial criteria) To improve survival in selected patients with LV dysfunction after an acute MI To assist management of diuretics induced hypokalemia (plasma potassium < 3. metabolic alkalosis.
5 mg TID of captopril. However. nitrates. Beta blocker. Control HR. or up to 4mg. ACEI. such as angina or HPN Felodipine does not affect mortality in HF v Indications for hospitalization Hypotensive with organ hypoperfusion Profound fluid retention states Substantive renal or hepativ insufficiency Hemodynamic instability requiring IV inotropes Dysrrhythmias requiring IV antiarrhythmics Decompensated HF with refractory angina Complication of post cardiac transplantation Elevated CPK and CPK-MB and/or ECG with ischemia/ injury or new necrosis Specialized Therapy for Refractory HF v Intravenous Inotropes and vasodilators IV Inotropes Norepinephrine Epinephrine Isoproterenol Dopamine Dobutamine Amrinone Milrinone IV vasodilators Nitroprusside Nitroglycerine v v v v Hemodynamic monitoring Pacemakers Hemofiltration Mechanical circulatory support Criteria for LV assist device implantation Ø Ø Ø Active heart transplant candidate On maximal inotropic support. rate control of AF Anti-HPN therapy. amlodipine and felodipine appear to be safe in patients with HF and can be used if treatment with a CACB is necessary for another indication. v ARBs ARBs for the treatment of HF appear to be as effective as. C Mechanical assist device Heart transplant Continuous IV inotropic infusion Hospice care Diagnostic Criteria for Diastolic Heart Failure v Signs and symptoms of CHF Exertional dyspnea Orthopnea Gallop sounds Lung crepitations Pulmonary edema v AND normal or mildly reduced LV systolic function v AND evidence of abnormal LV relaxation. Avoid atrial distension Anti-HPN therapy Anti-HPN therapy Exercise limitation.25 mg of captopril TID) then gradually increase to maintenance dose of 10mg BID of enalapril. Every 2 to 3 weeks) until the target dose is reached or symptoms become limiting v Digoxin Given to patients with HF and systolic dysfunction to control symptoms (such as fatigue. Morphine. in patients with atrial fibrillation. dyspnea.5 mg of enalapril BID or 6. to control the ventricular rate v CACB There is no direct role for these drugs in the management of HF.24 sec Second or third degree AV block Severe COPD History of asthma Severe peripheral vascular disease Begin therapy with low doses (eg. with or without intra aortic balloon pump Systolic pressure < 80mmHg with either: cardiac index <2L/m2 or PCWP < mmHg 6 Prognosis v Less than 50% of patients will survive for 5 years after the onset of heart failure v Sudden cardiac death is responsible for approximately 1/3 of deaths in patients with heart failure Lala 3C-Med-09 . distensibility. B. metoprolol and bisoprolol improve overall and event free survival in patient with NYHA class II to III HF and probably in class IV HF Beta blocker with intrinsic sympathomimetic activity (such as pinolol and acebutolol) should be avoided Relative contraindications for beta blockers in patients with HF Ø Ø Ø Ø Ø Ø Ø HR < 60 Systolic arterial pressure <100 mmHg PR interval > 0. beta blocker. or possibly slightly less effective than ACEIs when compared directly They should not be used in preference to ACEIs v Beta blockers Carvedilol. revascularization CACB? Beta blocker? ACEI? Beta blockers may lead to an increase in symptoms for 4 to 10 weeks before any improvement is noted. beta blockers. Atrial antiarrhythmics. Tourniquet.day of lisinopril or quinapril unless side effects occur v Surgery v Cardiac Transplantation Treatment of Associated Conditions v Supraventricular arrhythmias Rate control Restoration of sinus rhythm v Ventricular arrhythmias v Anticoagulation v Anemia Summary of Management v Stage A – High risk for developing HF but has no structural disorder of the heart Treat HPN Smoking cessation Treat dyslipidemia Discourage alcohol and illicit drug use ACEI in appropriate patients v Stage B – Structural disorder of the heart but who has never developed symptoms of HF All measures under stage A ACEI in appropriate patients Beta blockers in appropriate patients v Stage C – Past or current symptoms of HF associated with underlying structural heart disease All measures under stage A Drugs for routine use: diuretics. Salt Restriction Cardioversion of AF. and exercise intolerance) and. and diastolic stiffness Treatment of Diastolic Dysfunction Goals Reduce preload Maintain atrial contraction Enhance ventricular emptying Regression of hypertrophy Control heart rate Prevent and treat ischemia Improve myocardial relaxation Methods Venodilators. Therapy should be begun as very low doses and the dose doubled at regular intervals (eg. digitalis Salt restriction v Stage D – End stage disease who requires specialized treatment strategies All measures under stages A. cardioversion of AF. Diuretics. CACB. 2. filling.
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